MORC4 has recently been characterized as a breast cancer-associated anti-apoptotic oncoprotein. In the current study, we explored its downstream regulation in luminal A/B breast tumors.
Bioinformatic prediction was performed using data from The Cancer Genome Atlas (TCGA)-breast cancer (BRCA). Cellular and molecular studies were conducted using luminal A/B representative MCF-7 and BT-474 cell lines.
ENST00000355610.8 (encoding MORC4a isoform) was the dominant transcript in breast cancer. ChIP-qPCR and dual-luciferase assay confirmed two STAT3-binding sites in the promoter in both MCF-7 and BT-474 cells. Co-IP confirmed an interaction between MORC4 and STAT3. ChIP-qPCR data indicated that inhibition led to remarkably decreased enrichment of the STAT3-binding promoter segments. overexpression significantly elevated BCL-2 expression in MCF-7 cells and increased their resistance to adriamycin (ADM), 5-fluorouracil (5-FU), and cisplatin (DDP). inhibition largely abrogated MORC4-induced drug-resistance. However, the drug-resistant phenotype was rescued by overexpressing MID2-MT that was resistant to siRNA.
This study revealed a novel regulatory mechanism of MORC4 on expression via STAT3-mediated transcriptional activation. https://www.selleckchem.com/products/pki587.html This regulatory axis might confer increased chemoresistance to breast cancer cells.
This study revealed a novel regulatory mechanism of MORC4 on MID2 expression via STAT3-mediated transcriptional activation. This regulatory axis might confer increased chemoresistance to breast cancer cells.Lung cancer remains the leading cause of malignant tumor-related death globally. There is mounting evidence that a large proportion of patients harboring epidermal growth factor receptor (EGFR) mutation and treated with EGFR TKI experience oligoprogressive disease. The optimal treatment strategy for these patients is undetermined. Thus, in this article, we report two cases of EGFR-mutant NSCLC patients with locally resistant lesions achieving disease control via combination therapy.
We present two cases of lung adenocarcinoma patients that developed oligoprogressive disease during TKI treatment. For further treatment, the patient then received radiofrequency ablation.
Through follow-up observation, we found that the addition of radiofrequency ablation might provide the clinical benefit of these two NSCLC patients.
Our two cases provide a promising treatment for oligoprogressive disease during the first-line EGFR-TKI therapy.
Our two cases provide a promising treatment for oligoprogressive disease during the first-line EGFR-TKI therapy.Cutaneous squamous cell carcinoma (CSCC) is associated with a poor 5-year survival rate. circRNAs have an important role in a number of physiological and pathological processes. However, the relationship between circRNAs and cutaneous squamous cell carcinoma (CSCC) is unclear.
The aim of the present study was to investigate the expression of circRNAs in cutaneous squamous cell carcinoma (CSCC) and its effect on CSCC proliferation and metastasis.
We used high-throughput sequencing (RNA-seq) to identify circRNAs that were differentially in CSCC tissue and their paracarcinoma tissue. Quantitative real-time PCR results confirm deep-sequencing findings in CSCC tissue and cell lines. CCK-8 assay and flow cytometry were used to detect the effect of circPVT1 on the proliferation and migration of CSCC cells.
We identified 449 circRNAs that were differentially expressed between CSCC and normal adjacent tissue samples. circPVT1 (hsa_circ_0001821) was further researched to confirm its oncogene role in CSCC.
Differentially expressed circular RNA plays an important role in the development of CSCC, and circPVT1 may be an important target for the treatment of CSCC.
Differentially expressed circular RNA plays an important role in the development of CSCC, and circPVT1 may be an important target for the treatment of CSCC.At present, there are few studies on the mechanisms underlying postoperative recurrence of liver cancer, and the mechanism of action of in postoperative recurrence of liver tumors is not clear. Our goals were to investigate the effects of on the expression of the Ras-associated domain family 1A () gene and the regulation of primary and recurrent hepatic tumors to clarify the molecular mechanisms of in postoperative hepatocellular carcinoma.
We constructed a mouse liver orthotopic tumor model and a mouse liver recurrent tumor model. We measured the expression levels of the gene and then analyzed the effects of on the regulation of . We transiently transfected the gene into cells that stably overexpressed and examined relevant indicators to elucidate the mechanisms by which regulates the RASSF1A/c-Jun N-terminal kinase (JNK) pathway in recurrence and dormancy in liver cancer.
expression was inversely related to that of , activating transcription factor 2 (), and in SMMC7721 cells stably transfected with the gene and in recurrent mouse tumor tissues. After transient transfection of cells with mimic or inhibitor, the expression of was inversely related to that of .
might inhibit the JNK signaling pathway by inhibiting the expression of , thereby promoting recurrence of liver cancer after surgery. The low expression levels of in liver cancer tissues were closely related to postoperative recurrence; they could be used as a marker to judge the prognosis of patients with liver cancer.
MiR-602 might inhibit the JNK signaling pathway by inhibiting the expression of RASSF1A, thereby promoting recurrence of liver cancer after surgery. The low expression levels of miR-602 in liver cancer tissues were closely related to postoperative recurrence; they could be used as a marker to judge the prognosis of patients with liver cancer.Metastatic disease caused by prostate cancer (PCa) is the principal cause of PCa-related mortality. Long non-protein-coding RNAs may possess significant cellular functions. Plasmacytoma variant translocation 1 (PVT1), a long non-coding RNA encoded by the human gene, is an oncogene, which can regulate several tumor-related genes. In PCa, the function and mechanism of PVT1 are unclear. NOP2 is being pursued as a prognostic marker for cancer aggressiveness, which promotes mouse fibroblast growth and tumor formation. Essentially, nothing is known about the specific interactions between the PVT1 and NOP2.
190 pairs of PCa tissues and adjacent normal tissues were collected andRNA sequencing was used to identify the differential lncRNAs.Real-time quantitative real-time PCR (RT-qPCR) confirmed these results and gene regulatory relationship.Lentiviral vectors were used to alter PVT1 and genes to analyze their effects on PCa progression.Transwell migration and invasion assays were performed to test the metastasis ability.